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Published on: June 14, 2016
Pathological changes in ventricular false chordae tendineae in patients with dilated cardiomyopathy
Yaping Xu1,2, Chenlei Zhou2, Yuexin Yu1
1Henan Key Laboratory of Cardiac Remodeling and Transplantation, Zhengzhou Seventh People's Hospital, Affiliated with Xinxiang Medical University, Henan, PR China.
Objective:
To investigate the pathological changes in ventricular false chordae tendineae in patients with dilated cardiomyopathy (DCM).
Methods:
Gross anatomy, histology, immunohistochemistry, and immunofluorescence techniques were employed to examine the anatomical features, tissue composition, and the distribution of blood and lymphatic vessels in the false chordae tendineae of the left and right ventricles from six DCM patients and one normal heart. The expression and localization of the gap junction protein connexin 43 (Cx43) in the false chordae tendineae were also assessed.
Results:
False chordae tendineae were observed in both left and right ventricles, with a greater number found in the left ventricle. Based on histological characteristics observed with Masson's trichrome staining, false chordae tendineae were categorized into four types: muscular (cardiomyocytes), conductive (Purkinje fibers), mixed (both), and tendinous (dense connective tissue). The false chordae tendineae were surrounded by a thick connective tissue sheath, which extended inward to separate the internal cells into clusters or islands. Cx43 was abundantly expressed between cells, predominantly localized at the lateral-lateral regions, with fewer end-to-end connections. The interior of the false chordae tendineae was rich in blood and lymphatic vessels.
Conclusion:
In DCM patients, the gross morphology of ventricular false chordae tendineae showed no significant changes; however, marked proliferation of fibrous connective tissue was frequently observed, separating cardiomyocytes or Purkinje fibers into bundles or completely replacing the cellular components. This may contribute to the pathological basis of reentrant arrhythmias. Furthermore, the remodeling of Cx43 from an end-to-end to a lateral-lateral distribution may underlie electrical heterogeneity.
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